针刺太冲穴对自发性高血压大鼠延髓头端腹外侧区中NOX家族表达的影响

Effects of acupuncturing Taichong(LR3) on NOX family expression in rostral ventrolateral medulla of spontaneously hypertensive rats

目的:探讨针刺对自发性高血压大鼠(SHR)延髓头端腹外侧区(RVLM)中NADPH氧化酶同源物家族(NOX家族)表达的影响。方法:12只WKY大鼠为正常组,36只SHR大鼠随机分为模型组、针刺组和非穴组,每组12只。针刺组取太冲穴直刺,非穴组取非穴位浅刺,每天治疗1次,共14d。采用遥测技术检测血压;采用化学发光法检测RVLM中NADPH氧化酶活性;采用Real-time PCR检测RVLM中NOX家族同源物NOX1、NOX2(gp91phox)、NOX4的表达;采用Western Blot检测RVLM中NADPH氧化酶催化亚基gp91phox的表达。结果:与正常组比较,模型组大鼠平均动脉压显著增高(P<0.05);RVLM中NADPH氧化酶活性显著增高(P<0.05);NOX2(gp91phox)基因及蛋白表达水平显著增高(P<0.05)。与模型组和非穴组比较,针刺第8天可显著下调SHR大鼠的平均动脉压(P<0.05),针刺14d可下调RVLM中NADPH氧化酶活性(P<0.05),下调NOX2(gp91phox)基因及蛋白表达水平(P<0.05)。结论:针刺可显著改善SHR大鼠血压,其机制可能与下调RVLM中NOX2表达水平相关。

Objective： To investigate the effect of acupuncture on the expression of NADPH oxidase homolog（NOX family） in the rostral ventrolateral medulla（RVLM） of spontaneously hypertensive rats（SHR）. Methods： Twelve Wistar（WKY） rats were used as normal group, and 36 SHR rats were randomly divided into model group, acupuncture group and non-acupoint group. The acupuncture group took the Taichong（LR3） straight thorn, the non-acupoint group took the non-acupoint shallow thorn, and was treated once a day for 14 days. The effect of acupuncture on blood pressure was detected by telemetry. The effect of acupuncture on the change of NADPH oxidase activity in RVLM was detected by chemiluminescence method. The effect of acupuncture on the expression of NOX1, NOX2（gp91 phox） and NOX4 in NOV family in RVLM was detected by realtime PCR. Western Blot was used to detect the effect of acupuncture on the expression of NADPH oxidase catalytic subunit gp91 phox in RVLM. Results： Compared with WKY, SHR showed significant elevated MAP（P0.05）. Acupuncture for 8 days significantly decreased the MAP compared with SHR or Non-acupoint groups（P0.05）. The NADPH oxidase activity, the mRNA and the protein expression of NOX2（gp91 phox） was up-regulated in SHR compared with WKY（P0.05）, and down-regulated by14 days of acupuncture（P0.05）. Conclusion： Acupuncture can decrease the high blood pressure in SHR, and the mechanism probably is related to down-regulating NOX2 expression in RVLM.